ArticleDiabetes care2022
Evidence That Hypothalamic Gliosis Is Related to Impaired Glucose Homeostasis in Adults With Obesity.
Article in Diabetes care, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Hypothalamic Inflammaging: A Central Driver of Type 2 Diabetes Mellitus and Metabolic Disease in Aging.Diabetes & metabolism journal · 2026Review
- Acute anti-obesity treatment with celastrol reduces body weight, cerebral inflammation and metabolic imbalances in mice.Molecular medicine (Cambridge, Mass.) · 2026Article
- From diet to hypothalamic dysfunction: Neuroanatomical and hormonal integration of the microbiota-hypothalamus-adipose tissue axis.Reviews in endocrine & metabolic disorders · 2026Review
- High fat diet remodels the gene regulatory networks in the preoptic area.Scientific reports · 2026Article
- Astrocytes in systemic regulation of blood glucose and the development of type 2 diabetes.Frontiers in cellular neuroscience · 2026Review
- Assessing the physiology of weight loss based on real-time weight monitoring: The ADAPT behavioral weight loss study protocol.PloS one · 2026Article
- Hypothalamic Gliosis Is Associated With Multiple Cardiovascular Disease Risk Factors in the Framingham Heart Study.Journal of the American Heart Association · 2025Article
- Update on Hypothalamic Inflammation and Gliosis: Expanding Evidence of Relevance Beyond Obesity.Current obesity reports · 2025Review
- Hypothalamic neuronal-glial crosstalk in metabolic disease.npj metabolic health and disease · 2024Review
- Hypothalamic MRI-derived microstructure is associated with neurocognitive aging in humans.Neurobiology of aging · 2024Article
- In utero exposure to maternal diabetes or hypertension and childhood hypothalamic gliosis.International journal of obesity (2005) · 2024Article
- Glucose dysregulation in antipsychotic-naive first-episode psychosis: in silico exploration of gene expression signatures.Translational psychiatry · 2024Article
- A review of air pollution as a driver of cardiovascular disease risk across the diabetes spectrum.Frontiers in endocrinology · 2024Review
- Reduction of oxytocin-containing neurons and enhanced glymphatic activity in the hypothalamic paraventricular nucleus of patients with type 2 diabetes mellitus.Acta neuropathologica communications · 2023Article
- The Neurobiology of Eating Behavior in Obesity: Mechanisms and Therapeutic Targets: A Report from the 23rd Annual Harvard Nutrition Obesity Symposium.The American journal of clinical nutrition · 2023Article
- Review
- The Significance of Hypothalamic Inflammation and Gliosis for the Pathogenesis of Obesity in Humans.Endocrine reviews · 2023Review
- Exposure to Gestational Diabetes Mellitus Prior to 26 Weeks Is Related to the Presence of Mediobasal Hypothalamic Gliosis in Children.Diabetes · 2022Article
- Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative.Antioxidants (Basel, Switzerland) · 2022Review
- Glial Modulation of Energy Balance: The Dorsal Vagal Complex Is No Exception.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectivePreclinical research implicates hypothalamic glial cell responses in the pathogenesis of obesity and type 2 diabetes (T2D). In the current study we sought to translate such findings to humans by testing whether radiologic markers of gliosis in the mediobasal hypothalamus (MBH) were greater in individuals with obesity and impaired glucose homeostasis or T2D. RESEARCH DESIGN AND
methodsUsing cross-sectional and prospective cohort study designs, we applied a validated quantitative MRI approach to assess gliosis in 67 adults with obesity and normal glucose tolerance, impaired glucose tolerance (IGT), or T2D. Assessments of glucose homeostasis were conducted via oral glucose tolerance tests (OGTT) and β-cell modeling.
resultsWe found significantly greater T2 relaxation times (a marker of gliosis by MRI), that were independent of adiposity, in the groups with IGT and T2D as compared with the group with normal glucose tolerance. Findings were present in the MBH, but not control regions. Moreover, positive linear associations were present in the MBH but not control regions between T2 relaxation time and glucose area under the curve during an OGTT, fasting glucose concentrations, hemoglobin A1c, and visceral adipose tissue mass, whereas negative linear relationships were present in the MBH for markers of insulin sensitivity and β-cell function. In a prospective cohort study, greater MBH T2 relaxation times predicted declining insulin sensitivity over 1 year.
conclusionsFindings support a role for hypothalamic gliosis in the progression of insulin resistance in obesity and thus T2D pathogenesis in humans.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.